Original Research

published: 05 October 2016

doi: 10.3389/fneur.2016.00171

Positive association between

Tinnitus and arterial hypertension
Ricardo Rodrigues Figueiredo1,2*, Andréia Aparecida Azevedo1 and
Norma De Oliveira Penido1
1
 Otolaryngology, Universidade Federal de São Paulo, São Paulo, Brazil, 2 Otolaryngology, Faculdade de Medicina de
Valença, Valença, Brazil

Edited by:
Winfried Schlee,
University of Regensburg, Germany

Reviewed by:
Jae-Jin Song,
Seoul National University Bundang
Hospital, South Korea
Marzena Mielczarek,
Medical University of Lodz, Poland

*Correspondence:
Ricardo Rodrigues Figueiredo
rfigueiredo@otosul.com.br

Specialty section:
This article was submitted to
Neuro-otology,
a section of the journal Keywords: tinnitus, arterial hypertension, hearing loss, cardiovascular diseases, hearing disorders
Frontiers in Neurology

Received: 23 June 2016
Accepted: 21 September 2016
INTRODUCTION
Published: 05 October 2016
Tinnitus is the perception of noise, which is not generated by external stimulus (1). It affects approxi-
Citation: mately 25% of the general population: one third on a frequent basis (2). Tinnitus may be classified as
Figueiredo RR, Azevedo AA and
auditory and para-auditory tinnitus with the former representing the majority of cases, and the latter
Penido NO (2016)
Positive Association between
being subdivided into muscular and vascular tinnitus, sometimes referred as somatosounds (3).
Tinnitus and Arterial Hypertension. According to the most recent trends of thought, tinnitus is considered a symptom which may
Front. Neurol. 7:171. have multiple causes, sometimes even in a single patient (4, 5). Noise exposure, metabolic and car-
doi: 10.3389/fneur.2016.00171 diovascular disease, presbycusis, ototoxicity, and cranial and cervical trauma are the most frequently

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Figueiredo et al.
considered causes of tinnitus (5, 6). Caffeine abuse, dietary fac-
tors, temporomandibular joint, and cervical disease have also
been described as contributing factors (7–9).
Systemic arterial hypertension is a multifactorial clinical
condition characterized by raised and sustained arterial pressure
levels (10). It is defined as systolic levels equal or greater than
140 mmHg and diastolic levels equal or greater than 90 mmHg
(10). The prevalence in Brazil, similar to that in other countries, is
estimated to be between 22.3 and 43.9% (32.5% average), raising
to 50% between 60 and 69 years old and 75% for 70 years and older
(10–12). The presence of comorbidities, such as diabetes mellitus
and dyslipidemias, and habits, such as smoking, was demonstrated
to increase complications risks (13). Arterial hypertension has been
described as a possible cause of tinnitus since 1940s (14). Three
principle mechanisms suspected of being involved are: damage to
inner ear microcirculation (15), ototoxicity by antihypertension
drugs (16), and perception of noise generated by blood vessels (3).
As related to inner ear microcirculation, the stria vascularis
was demonstrated to be the main cochlear site damaged by arte-
rial hypertension (17). Sodium retention could also lead to an
increase of extracellular fluid volume, including the perilymph
(18), and the endocochlear potential being reduced in hyperten-
sive rats (19). Moreover, hypertension has been associated with a
higher risk of hearing loss in brain ischemia (15) and also with a
slower recovery in sudden hearing loss (20).
In considering ototoxicity, an extensive review cited diuretics,
beta-blockers, angiotensin-conversing enzyme (ACE) inhibitors,
angiotensin II receptors blockers, and calcium channels blockers
as possible ototoxic medications (21). Furosemide’s ototoxicity is
the most studied form, producing a quick and reversible decrease
of the endocochlear potential (22).
As for vascular tinnitus, some studies cite hypertension as
a causal factor, mainly when vascular abnormalities have been
ruled out (3). An anatomopathological study demonstrated a
high incidence of bony dehiscence of the carotid canal in the
middle ear, which may affect the inner ear microcirculation and
also generate vascular noises (23).
According to a systematic review, there is evidence of an
association between tinnitus and arterial hypertension, but there
is a lack of more comprehensive studies (24). The association is
stronger in studies that analyzed the presence of arterial hyper-
tension in patients with tinnitus than in those which analyzed the
presence of tinnitus in patients with arterial hypertension.
The main purpose of this study is to analyze the presence of arte-
rial hypertension in tinnitus and non-tinnitus patients. Secondary
purposes are to analyze differences between tinnitus impact and
psychoacoustic measurements in hypertensive and normotensive
patients and to evaluate the association between the presence of
tinnitus and the diverse antihypertensive drugs employed.
MATERIALS AND METHODS
This is a transversal case–control study in which individu-
als of 18  years of age or older with and without tinnitus were
selected at the author’s ENT clinic from 2011 to 2014. The trial
was approved by the Institutional Review Board (number 010/
CEP-FMV/2011). This study was carried out in accordance
Frontiers in Neurology  |  www.frontiersin.org
Tinnitus and Hypertension
with the recommendations of the aforementioned Institutional
Review Board with written informed consent from all subjects.
All subjects gave written informed consent in accordance with
the Declaration of Helsinki.
Two groups were created: the first included patients with tinni-
tus of at least 3 months duration and the second included patients
without tinnitus (control). The control group was paired with the
tinnitus group for gender, age, and race. The time of tinnitus onset as
related to arterial hypertension onset was not an exclusion criteria.
Patients from both groups were submitted to anamnesis (including
demographics, comorbidities, and habits), otorhinolaryngological
physical examination, and arterial pressure measurements with a
calibrated sphygmomanometer (Erka Perfekt Aneroid, Germany),
in order to exclude possible undiagnosed arterial hypertension.
The criteria for blood pressure evaluation were those from the VII
Joint National Committee on Prevention, Detection, Evaluation,
and Treatment of High Blood Pressure, U. S. Department of Health
and Human Services, as previously described.
Patients allegedly normotensive with high blood pressure
detected at the physical examination were excluded. Patients
from both groups also underwent conventional pure tone and
speech audiometry.
Tinnitus patients were questioned regarding their tinnitus
characteristics (duration, type of sound, laterality, and periodic-
ity) and also classified their tinnitus according to a Visual Analog
Scale (VAS), from 1 to 10 (for intensity and distress) and to the
Brazilian Portuguese validated version of the Tinnitus Handicap
Inventory (THI) (25). They also underwent psychoacoustic meas-
urements of their tinnitus – Pitch Matching (PM) and Minimum
Masking Level (MML).
The sample size was determined after the analysis of the arte-
rial hypertension prevalence in a preliminary sample of tinnitus
patients (n = 46) that was compared to the prevalence of arterial
hypertension in the Brazilian general population, obtained from
previous studies (10). The minimum number of individuals for
each group was determined to be 140.
For whole sample analysis, the comparison of the variables
between the tinnitus group and the control group was performed
using the Mann–Whitney test for the numerical data and the chi-
square or the Fisher test for the categorical data. The Spearman
coefficient was performed to analyze the association between the
duration of arterial hypertension and the numerical audiometry
measurements. The Cochran–Mantel–Haenszel was used to ana-
lyze the association between tinnitus and arterial hypertension
adjusting for the presence of hearing loss. The significance level
was established at 5%, and the statistical analysis was performed
with the SAS statistical software, 6.11 version (SAS Institute, Inc.,
Cary, NC, USA).
RESULTS
The final sample was composed of 144 patients in the tinnitus
group and 140 in the control group. The tinnitus group was then
divided into two subgroups: one for patients with arterial hyper-
tension and the other without arterial hypertension.
The average age was 57.8 years of age for the tinnitus group
and 58.6 for the control group. The averages of tinnitus duration,
2 October 2016 | Volume 7 | Article 171
Figueiredo et al. Tinnitus and Hypertension

VAS for intensity, VAS for distress, and THI scores for the tinnitus
group were, respectively, 54.5 months–4.5 years, 5.45, 5.83, and
41.7 points.
Although the duration of arterial hypertension was longer
(average of 128.7 months–10.7 years) than the duration of tinnitus
(average of 54.5 months), no statistically significant correlation
was found, according to the Spearman coefficient. Considering
the patients that could ascertain the duration of both arterial
hypertension and tinnitus (n = 56), for 42 of them (75%) arterial
hypertension preceded tinnitus.
Table  1 shows the comparison of numerical variables and
Table 2 shows the categorical variables, the latter confirming the
pairing by gender, age, and race. As shown in Table  2, arterial
hypertension was more prevalent in tinnitus patients (p = 0.024),
demonstrating an association of tinnitus and arterial hyperten-
sion. This association was not found when data were adjusted for
the presence of hearing loss (p = 0.27, according to the Cochran–
Mantel–Haenszel test). Hearing loss was more frequent in the
tinnitus group, as shown in Table 3, but there was no difference
between the two groups as to the type of hearing loss or the shape
of the audiogram curve. Sensorineural descendant was the most
frequent curve in both groups (75% in the tinnitus patients group
and 58% in the control group). Also, there was no difference in the
speech recognition index of both groups (100% median in both).
Table 1 | Analysis of the numerical variables (age, duration of arterial
hypertension, and daily consumption of caffeine) according to the group.
The analysis of the antihypertensive drugs used in both groups
is shown in Table 4.
The analysis of comorbidities and habits demonstrated that
dyslipidemia was more frequent in the tinnitus group (p-value of
0.003), while the presence of diabetes mellitus, hypothyroidism,
noise exposure, caffeine consumption, and smoking was similar
in both groups. When considering the coexistence of arterial
hypertension and comorbidities and habits, the association of
arterial hypertension and caffeine consumption greater than
150 milliliters per day was more frequent in the tinnitus group
(p < 0.0001).
Table 4 shows data about the antihypertensive drugs used in
both groups.
Table  5 shows data from the numerical variables for the
tinnitus’ patients subgroups, those with and without arterial
hypertension.
There was no statistical difference between the two subgroups
concerning gender and race. Diabetes mellitus and dyslipidemia
were more frequent in the subgroup with tinnitus and arterial
hypertension (p  =  0.017 and 0.02, respectively), while there
were no differences concerning hypothyroidism, noise exposure,
caffeine consumption, or smoking. Hearing loss was considered
to be more prevalent in the subgroup with arterial hypertension
(89.1%), although it was also frequent in the normotensive sub-
group (75%, p = 0.032). No differences concerning the type or
curve were found.

Variable Tinnitus No tinnitus p-Value Table 3 | Prevalence of hearing loss among tinnitus and non-tinnitus
patients (χ2 test).
n Median IQA n Median IQA
Variable Category Tinnitus No Tinnitus p-Value
Age (years) 144 59 49–69 140 58 50–67 0.97
N (ears) % N (ears) %
Arterial 60 120 39–216 43 180 84–240 0.019
hypertension Hearing Yes 111 81.3 75 53.6 <0.0001
duration loss No 32 18.7 65 46.4
(months)
Caffeine 144 100 50–200 140 300 200–400 0.0001
(ml/day) Table 4 | Analysis of the categorical variable – antihypertensive drugs
used according to the groups.
Significant values in bold.
IQA, Interquartilic Amplitude: Q1–Q3. Variable Category Tinnitus No tinnitus p-Value

Table 2 | Analysis of categorical variables (gender, age, race, and n % n %

presence of arterial hypertension) according to the groups.
B-blocker Yes 19 13.2 21 15.0 0.66
Variable Category Tinnitus No Tinnitus p-Valuea No 125 86.8 119 85.0
ACEI Yes 23 16.0 8 5.7 0.006
n % n % No 121 84.0 132 94.3

Gender Male 62 43.1 65 46.4 0.57 ARB Yes 34 23.6 24 17.1 0.18
Female 82 56.9 75 53.6 No 110 76.4 116 82.9

Age (years) ≤40 18 12.5 14 10.0 0.82 Loop Yes 0 0.0 4 2.9 0.057
41–59 55 38.2 60 42.9 diuretic No 144 100.0 136 97.1
60–69 40 27.8 36 25.7 Thiazidic Yes 29 20.1 8 5.7 <0.0001
≥70 31 21.5 30 21.4 diuretic No 115 79.9 132 94.3
Race White 93 71.5 98 70.0 0.94 K sparing Yes 6 4.2 0 0.0 0.016
Brown 22 16.9 24 17.1 diuretic No 138 95.8 140 100.0
Black 15 11.5 18 12.9
CCA Yes 13 9.0 2 1.4 0.004
Arterial Yes 64 44.4 44 31.4 0.024 No 131 91.0 138 98.6
Hypertension No 80 55.6 96 68.6
χ-squared or Fisher tests.
Significant values in bold. ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker;
χ or Fisher test.
a 2
CCA, calcium channel antagonist.

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Figueiredo et al. Tinnitus and Hypertension

Table 5 | Analysis of the numerical variables (age, caffeine consumption, Table 6 | Analysis of the categorical variables (tinnitus clinical
tinnitus duration, Visual Analog Scale, Tinnitus Handicap Inventory, Pitch characteristics) according to the tinnitus’ patients’ subgroups (with and
Masking, and Minimum Masking Level) according to the subgroups of without arterial hypertension).
tinnitus patients (with and without arterial hypertension).
Variable Category Arterial No arterial p-Valuea
Variable Arterial No arterial p-Valuea hypertension hypertension
hypertension subgroup hypertension subgroup subgroup subgroup

n Median IQA n Median IQA n % n %

Age 64 66 57–72 80 52.5 43–65 0.0001 Laterality RE 13 20.3 22 27.5 0.60

(years) LE 15 23.4 14 17.5
Caffeine 58 100 50–200 67 100 100–200 0.78 Bilateral 32 50.0 41 51.3
(ml/day) Head 4 6.3 3 3.8

Tinnitus 59 24 9–60 76 18 5.3–60 0.22 Instalation Sudden 33 55.0 33 42.9 0.0.16

duration Gradual 27 45.0 44 57.1
(months) Periodicity Constant 45 70.3 55 69.6 0.93
VAS 63 5 3–7 80 6 4–8 0.37 Intermittent 19 29.7 24 30.4
volume χ or Fisher test.
a 2

(points) RE, right ear; LE, left ear.

VAS 63 5 3–8 80 6 4–9 0.37
distress
attempt to establish a correlation between arterial hypertension
(points)
and tinnitus studies will help to elucidate characteristic in com-
THI score 63 40 18–70 80 38 16.5–61.5 0.75
(points)
mon that could be addressed in the diagnosis and therapeutic
interventions. However, causal correlate studies would demand a
PM RE 40 4000 1000–8000 64 6000 2000–8000 0.58
(Hz)
plethora of different cases, including patients without tinnitus or
PM LE 45 4000 1500–8000 56 6000 3250–8000 0.27
arterial hypertension who were also free from other infirmities or
(Hz) habits which could be linked to tinnitus generation. Oftentimes,
MML RE 40 15 5–25 63 15 10–30 0.36
this elaborate type of study requires an extensive time period and
(dB SL) patients with incredibly varied conditions.
MML LE 44 15 5–29 55 15 5–25 0.48 A systematic review on this subject (24) argued that studies
(dB SL) which have evaluated the prevalence of tinnitus among hyper-
Nineteen patients reported no caffeine consumption, nine patients could not estimate
tensive patients failed to demonstrate an association (26–29).
the duration of their tinnitus, and one patient could not report VAS and THI scores. However, data from this study, along with other studies (2, 30, 31),
IQA, interquartilic amplitude: Q1–Q3. demonstrated an association between tinnitus and arterial hyper-
Bold is to highlight the significant data. tension (hypertension prevalence in tinnitus patients  =  44.4%
a
Mann–Whitney test.
VAS, Visual Analog Scale; THI, Tinnitus Handicap Inventory; PM, Pitch Masking;
against 31.4% in patients without tinnitus, p = 0.024).
MML, Minimum Masking Level; RE, right ear; LE, left ear; dB, decibel; dB SL, decibel The information above may lead one to infer that tinnitus
Sensation Level. could be a causal factor for hypertension, albeit it seems more
reasonable to believe arterial hypertension is more a cofactor than
a main cause of tinnitus.
Table 6 shows the tinnitus characteristics in both subgroups. Regarding hearing loss, the results are in conformity with
The most frequently described types of tinnitus were wheezing, prior studies, which found a high prevalence among tinnitus
whistle, and insect with no differences between the subgroups. patients, as well as the higher prevalence of sensorineural pattern
The presence of multiple types of sound in the same patient was with descending configuration curves (2, 5).
more frequently found in the hypertensive subgroup (p = 0.014). Once hearing loss was added to (adjusted for) the statistical
The prevalence of vascular tinnitus was 6.3% in the hypertensive analysis, the association between tinnitus and arterial hyperten-
subgroup and 1.3% in the normotensive one (p  =  0.12) with sion was no longer positive, suggesting that arterial hypertension
muscular tinnitus being found in only two cases, both being in may be a cause of hearing loss, which is related to most cases
normotensive patients. of tinnitus, as previously reported (1, 6). Having said so, if we
No significant differences were found between the subgroups think about tinnitus prevention, arterial hypertension may still
concerning the otolaryngologic exam, including evaluation of be regarded as a possible important causal factor.
the temporomandibular joint. Finally, there was no correlation Arterial hypertension may affect the inner ear microcircula-
discovered between the duration of arterial hypertension and tion, and it is known that comorbidities, such as diabetes mellitus
tinnitus according to the Spearman coefficient (p = 0.77). and dyslipidemia, may enhance vascular impairment due to
hypertension (10). Although dyslipidemia was more prevalent in
DISCUSSION the tinnitus group, there was no difference concerning the con-
comitancy of arterial hypertension and dyslipidemia. Diabetes
Association studies are key sources of information for the com- mellitus also affects the inner ear microcirculation, but it may
prehension of how one disorder may affect another. A study on also have direct metabolic effects on cochlea (4, 5, 20). There

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Figueiredo et al.
was a statistical tendency in favor of a higher prevalence of the
concomitancy of diabetes and hypertension in the tinnitus group.
As for hypothyroidism, another metabolic disease frequently
cited as related to tinnitus (6), no differences between the two
groups were found, either as an isolated factor or in association
with arterial hypertension. The comparison between the tin-
nitus subgroups (with and without hypertension) demonstrated
that diabetes mellitus and dyslipidemia were more prevalent in
hypertensive tinnitus patients, suggesting that these diseases
may act synergically upon the generation, maintenance and/or
aggravation of tinnitus.
The excessive consumption of caffeine is believed to have a
negative impact on hypertension control (32), but its association
with tinnitus has been doubted by recent studies (9, 33, 34). Data
from this study failed to demonstrate any association between
tinnitus and caffeine consumption. In fact, the concomitancy of
hypertension and caffeine intake greater than 150 ml per day was
more prevalent in the control group, which may reflect the wide-
spread patients’ concept that caffeine worsens tinnitus. Smoking,
which is believed to worsen both tinnitus and hypertension,
probably by impairing macro and microcirculation (10, 35), was
more prevalent in the tinnitus group, either as an isolated factor
or concomitant to hypertension.
Considering these findings, one might speculate that vascular
changes, which may affect cochlear microcirculation, leading to
hair cells damage and, consequently, tinnitus is probably a com-
mon pathophysiological scenario for many conditions, such as
arterial hypertension, dyslipidemia, diabetes mellitus, smoking,
and caffeine abuse. These conditions are not infrequently found
in a single patient and may act sinergically, multiplying the dam-
age to the auditory system.
Although noise exposure is considered as one of the main
causes of tinnitus (4, 6), data from this study failed to establish
an association between noise exposure and tinnitus, either
isolated or concomitant to hypertension. This finding should be
considered with caution, being that the study was performed in
an industrial city where many workers are exposed to industrial
or recreational noise.
The average age of patients with tinnitus and arterial hyperten-
sion was significantly higher than the age of those in the group
with tinnitus and no arterial hypertension. In the hypertension
tinnitus subgroup most of the patients were 60  years or older,
while the opposite was verified in the subgroup without hyper-
tension. Both tinnitus and arterial hypertension are more preva-
lent in the elderly (2, 10), but these findings may also be due to
some synergistic action of presbycusis and arterial hypertension
contributing to tinnitus generation and, eventually, aggravation.
The difference concerning arterial hypertension duration,
which was significantly lower in the tinnitus group, may be due
to a lack of proper control of blood pressure in the first years,
which may lead to perfusion and reperfusion vascular events in
the cochlea. More studies are needed to clarify these findings.
The median of the pitch masking was higher (6 kHz) in the
subgroup without hypertension than when compared to the
hypertension subgroup (4  kHz), although this difference was
not statistically significant. Both measures are in agreement with
most of the references, tinnitus ranging from 3 to 8 kHz, which
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Tinnitus and Hypertension
corresponds to the usually most affected frequencies in hearing
loss (36, 37). As for the MML, the averages of both subgroups were
the same (15 dB SL), which is somewhat higher than the usually
reported sensation level of 5–10 dB SL (37). No differences were
demonstrated concerning the degree of intensity and distress due
to tinnitus in both subgroups, considering the VAS and the THI.
The tinnitus’ characteristics were similar in both groups,
including the type of sound perceived by the patients. The fact that
multiple sounds’ tinnitus was more prevalent in the hypertensive
patients may reflect the multicausality of tinnitus, hypertension
being one of the possible factors involved.
Although the average duration of arterial hypertension was
longer than the duration of tinnitus and for most of the patients
the onset of hypertension preceded the onset of tinnitus, the
methodology of this case–control does not allow the conclusion
that hypertension is a causal factor for tinnitus.
The ototoxicity of many antihypertension medications has
been well established, especially with diuretics (21, 22). Data
from this study demonstrated that the use of ACE inhibitors,
thiazidic diuretics, potassium-sparing diuretics, and calcium
channels blockers was more prevalent in the tinnitus hypertensive
patients than in the control group. These findings have a partial
correspondence with prior studies (16) and, although they are
not strong enough to justify a correlation between an eventual
ototoxicity of these drugs and the presence of tinnitus (for
example, multidrug therapy for hypertension is very frequent), it
appears that further, more detailed studies on this subject should
be performed.
CONCLUSION
There is an association between tinnitus and arterial hyperten-
sion. This association is particularly strong in older patients
and cannot be dissociated from the hearing loss, which was also
more prevalent among tinnitus patients. The use of thiazidic and
potassium-sparing diuretics, ACE inhibitors, and calcium chan-
nels blockers was more prevalent in tinnitus patients.
The clinical and psychoacoustic characteristics of tinnitus in
hypertensive and normotensive patients were similar, as well as
tinnitus-related distress.
AUTHOR CONTRIBUTIONS
RF – study design, data collection, and writing. AA – data collec-
tion. NP – study design and writing.
ACKNOWLEDGMENTS
Rosângela Martins, for the statistics. Lisa Morrison Thuler, for the
manuscript English revision.
FUNDING
This work was supported by a grant from CAPES – Coordenação
de Aperfeiçoamento de Pessoal de Nível Superior – Governo
Federal do Brasil.
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Figueiredo et al.
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Conflict of Interest Statement: The authors declare that the research was con-
ducted in the absence of any commercial or financial relationships that could be
construed as a potential conflict of interest.
Copyright © 2016 Figueiredo, Azevedo and Penido. This is an open-access article
distributed under the terms of the Creative Commons Attribution License (CC BY).
The use, distribution or reproduction in other forums is permitted, provided the
original author(s) or licensor are credited and that the original publication in this
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6 October 2016 | Volume 7 | Article 171